Fine-particulate matter aggravates cigarette smoke extract-induced airway inflammation via Wnt5a-ERK pathway in COPD.

摘要: Background Exposure to environmental particulate matter (PM) ≤2.5 μm in diameter (PM2.5) and smoking are common contributors COPD, pertinent research implicates both factors pulmonary inflammation. Using vivo mouse vitro human cellular models, we investigated the joint impact of PM2.5 pollution, cigarette smoke (CS) mice or cigarette-smoke extract (CSE) cells on COPD inflammation, explored potential mechanisms. Methods Tissue changes lungs C57BL/6 exposed CS were studied by light microscopy, H&E, immunochemistry, immunofluorescence-stained sections. Levels inflammatory induced PM2.5/CS PM2.5/CSE 16HBE also monitored quantitative reverse-transcription (qRT)-PCR ELISA. Expression genes related Wnt5a-signaling pathway was assessed at transcriptional protein levels using immunofluorescence, qRT-PCR, Western blotting. Results Inflammatory response combined exposure CSE surpassed responses incited separately. Although separate CS/CSE upregulated expression Wnt5a (a member Wnt-secreted glycoprotein family), produced a steeper rise levels. Use antagonist (BOX5) successfully blocked effects. ERK phosphorylation appeared mediate effects model, promoting aggravation CS/CSE-induced airway Conclusion Our findings suggest that induce inflammation cells. Furthermore, seems aggravate via Wnt5a-ERK context COPD.